Abstract:We studied the influence of Withania somnifera (Ws) root extract (100 mg/kg body weight) on parkinsonism induced by 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP; i.p, 20 mg/kg body weight for 4 days), via the analysis of behavioral features and the oxidant-antioxidant imbalance in the midbrain of mice. A significant alteration in behavior, increased levels of thiobarbituric acid reactive substance (TBARS), and increased activities of superoxide dismutase (SOD) and catalase (CAT) were noticed in this region of brain in MPTP-treated mice. Oral treatment with the root extract resulted in a significant improvement in the mice's behavoiur and antioxidant status, along with a significant reduction in the level of lipid peroxidation. The results indicated that at least part of the chronic stress-induced pathology may be due to oxidative stress, which is mitigated by Ws. Further studies are needed to assess the precise mechanism to support the clinical use of the plant as an antiparkinsonic drug.

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Cyclooxygenase is the enzyme responsible for the production of prostaglandins (PGs). This cyclooxygenase exists in two isoforms: cyclooxygenase-1 (COX-1) and cyclooxygense-2 (COX-2). In humans and primates high levels of COX-2 are detected in the seminal vesicle. Further, the main source of PGs in the semen of these species is from the seminal vesicle. In rodents, the source of PGs in semen is from the vas deferens and abundant levels of COX-2 are detected. A direct relation is thought to exist between COX-2 levels and the source of PGs in semen. Moreover, the role of COX-1 and COX-2 in the seminal vesicle of rodents is obscure. The present study aims at localizing COX-1 and COX-2 in the seminal vesicle of mice. Immunohistochemical staining and COX activity assay revealed COX-1 as a dominant isoform in the mouse seminal vesicle. On treatment with nimesulide -a preferential COX-2 inhibitor -no change in staining intensity and COX activity was observed. The total PG levels also appeared to be unaltered following nimesulide treatment. This confirms that nimesulide had no effect on COX-1. The results presented here suggest COX-1 is the dominant isoform in the mouse seminal vesicle and is responsible for PG synthesis.